The interaction between TAMs and immune checkpoint inhibitors and other components of TME leads to the inhibition of immune checkpoints such as PD-1/PD-L1 and CTLA-4, resulting in the elimination of inhibitory signals for T cell activation, thus enabling tumor reactive T cells to overcome regulatory mechanisms and produce effective antitumor responses, known as the expression pattern of checkpoint molecules (49, 50). This evidence concerns the gene PDCD1 and neoplasm.